MPN
Myeloproliferative neoplasms (MPNs) are rare cancers and include diseases of the blood and bone marrow. MPNs involve dysregulation at the multipotent hematopoietic stem cell (CD34). MPNs occur when the bone marrow produces too many red blood cells, platelets, or certain white blood cells. The primary subtypes include myelofibrosis, polycythemia vera, and essential thrombocythemia.
Advertisement
Advertisement
New therapies, such as TP-3654, are currently being explored in combination studies.
Three of four patients with myelofibrosis had objective responses at one year, and no dose-limiting toxicities were observed.
No significant differences in HSCT were observed, suggesting haploidentical HSCT as an acceptable treatment approach.
AI-driven quantitative analysis was compared with manual evaluation of bone marrow trephine slides in a phase II trial.
Julie Braish, MBBCh, discusses her study on JAK2 allele burden in myelofibrosis presented at ASCO 2024.
Dr. Rampal, of Memorial Sloan Kettering Cancer Center, discusses his abstract at the EHA 2024 Congress in Madrid, Spain.
MPN depend on mutated JAK signaling, and targeting the mutations suppressed disease features and improved overall survival.
Pelabresib plus ruxolitinib improved spleen and symptom responses in JAKi-naïve patients with myelofibrosis.
Treatment with luspatercept improved transfusion burden and anemia across four cohorts of patients with myelofibrosis.
Prefibrotic PMF is an MPN with distinct characteristics comprising histopathological, clinical, and biological parameters.
Prefibrotic myelofibrosis is the focus of “SOHO State of the Art Updates and Next Questions.”
Momelotinib achieved higher rates of transfusion independence compared with ruxolitinib.
Splenic irradiation before HSCT is associated with reduced spleen size and lower incidence of relapse in patients with MF.
Sotatercept monotherapy, and combined with ruxolitinib, is a safe and effective treatment for patients with PMF and anemia.
Raajit Rampal, MD, PhD, and the "Blood Cancer Talks" hosts discuss the diagnosis and management of essential thrombocythemia.
The primary endpoint was overall best response after blast-reduction therapy.
Momelotinib and ruxolitinib improved bone marrow fibrosis, but changes were not associated with improved outcomes in MF.
Dr. Harrison discusses her current clinical research, building community with MPN Voice, and her journey into hematology.
A drug approval specific to CMML would catalyze a surge of interest in the hematology-oncology community.
Nicolaus Kröger, MD, discusses a study on GVHD and its impact on relapse in patients with myelofibrosis undergoing HSCT.
Myelofibrosis, a rare blood cancer, affects four to six per 100,000 individuals in the United States.
An international working group collaborating with the EBMT and ELN updated the 2015 guidelines for HSCT in myelofibrosis.
Ruxolitinib plus pelabresib was well tolerated and improved spleen and symptom burden in patients with myelofibrosis.
Parsaclisib plus ruxolitinib can improve symptoms and spleen volume in certain patients with myelofibrosis.
Sanjay Patel, MD, discusses a study on spatial mapping of human hematopoiesis using bone marrow tissue.
FREEDOM2 is a phase III study comparing fedratinib with best available therapy as a second-line treatment for myelofibrosis.
“Among the high-risk splicing mutations, SRSF2 has the worst prognostic role,” Dr. Braish and colleagues wrote.
The REVEAL study identified five risk factors, including leukocytosis, duration of time with PV, and more.
The treatment led to reduced hepcidin levels when used alone or in combination with ruxolitinib.
Venugopal highlights myelofibrosis research at ASH 2023.
Real-world databases lent insight into how often patients with PV experience thromboembolic events.
Dr. Al-Ali covers data on combined BET and JAK inhibition for patients with myelofibrosis presented at the 2023 ASH Meeting.
Worse survival in single-hit TP53 patients was mainly driven by bone marrow fibrosis.
SRSF2 and SF3B1 were the most common splicing mutations, followed by U2AF1 and ZRSR2.
Knowing who is at high risk in the near term could make it easier to conduct trials of anti-thrombotic therapies.
Developed by Protagonist Therapeutics, rusfertide is a novel injectable synthetic mimetic of the natural hormone hepcidin.
CALR and MPL mutations, which are associated with better outcomes, showed earlier mutation clearance than JAK2.
The retrospective study used data on 105 million U.S. patients with linked medical and prescription claims from 2007 to 2019.
Mass spectrometry–based proteomics were used to learn more about how MKs drive bone marrow fibrosis.
Prevalence of symptoms was assessed with the Myeloproliferative Neoplasm Symptom Assessment Form Total Symptom Score.
The retrospective study evaluated if pacritinib increased PLT counts in the phase III PERSIST-2 and phase II PAC203 studies.
Tasquinimod inhibited interaction of A9, a protein associated with poor prognosis.
DT2216 alone was effective, but exhibited a slightly greater cell viability reduction when combined with other therapies.
Responses in hemoglobin, white blood cell, and platelet were 75%, 82%, and 74%, respectively, at 24 weeks.
Multivariable modeling showed a notable reduction in the risk of GVHD or relapse in the ATG group.
Hemoglobin and platelets are correlated with OS, while mutations in ASXL1, EZH2, IDH1/2, U2AF1, and SRSF2 are not.
Rusfertide quickly induced hematocrit control and maintained improved levels over time in patients with polycythemia vera.
Subjectivity of morphological assessment and overlapping pathological features of subtypes can hamper accurate MPN diagnosis.
Bomedemstat is an oral lysine-specific demethylase-1 (LSD1) inhibitor clinically active in patients with MPNs.
The model could be helpful in understanding fibrotic progression in JAK2V617F mutation–positive MPNs.
Blood Cancers Today delivers the latest news, education, and information relevant to hematologic oncology patients and practices.
Sign up to receive Blood Cancers Today eNewsletters:
